Acute coronary syndromes, including unstable angina pectoris (UAP), are associated with a high morbidity and mortality. In general, UAP results from erosion or rupture of a vulnerable atherosclerotic plaque superimposed by occlusive thrombus formation and distal ischemia1. Atherosclerosis is increasingly regarded as a dyslipidemic disorder with a strong inflammatory character2. These inflammatory processes are in part orchestrated by chemokines, which participate in the inflammatory process by mediating monocyte recruitment to sites of injury, vascular smooth muscle cell proliferation, neo-vascularisation and platelet activation3-5. Furthermore, chemokines appear to play a role in cardiac ischemia as well. Indeed ischemia was reported to lead to induced expression of chemokines in the myocardium or in the circulation, translating in the recruitment of leukocyte subsets and progenitor cells to the injury zone to contribute to the injury repair6. Given their diverse and deep impact in cardiovascular diseases, chemokines might not only serve as biomarkers of atherosclerosis, plaque disruption or ischemia, but also represent attractive therapeutic targets7.
Approximately 50 chemokines have thus far been characterized and various are seen to be implicated in atherosclerosis and atherothrombosis5. In fact plasma levels of Regulated on Activation Normally T-cell Expressed and Secreted (RANTES or CCL5), Fractalkine (CX3CL1) and Monocyte Chemotactic Protein 1 (MCP-1 or CCL2) have already been shown in various studies to be altered in UAP or myocardial infarction8-11. Nevertheless, prospective data on chemokine plasma levels and/or chemokine receptor expression by circulating leukocyte subsets in acute coronary syndromes are lacking. Moreover, the use of such chemokines as markers of future coronary events has hitherto not been explored.